The contribution of incomplete myocardial relaxation and persistent interaction of contractile elements throughout diastole to increased left ventricular (LV) diastolic pressure in various diseases of the heart is uncertain. In the proposed studies, we will examine the mechanisms responsible for the abnormal LV diastolic compliance and relaxation seen during angina pectoris. Specifically, we plan to use an animal model (coronary stenosis plus increased 02 demand imposed by stress of pacing tachycardia) developed by us in an effort to closely approximate the physiology of angina pectoris, to answer 9 questions: (1) In this model, is the previously described upward shift in LV diastolic pressure-volume relations accompanied by an increase in Lv diastolic pressure relative to ischemic myocardial segment length, indicating decreased distensibility of the ischemic segment itself? (2) Alternatively, is the upward shift due to dyssynchronous wall motion with delayed contraction and/or elastic recoil of the ischemic segment during diastole? (3) Are there major differences between the diastolic physiology of angina (coronary stenosis-increased demand) and that of coronary occlusion in the same animal? (4) Is intrinsic myocardial stiffness (stiffness-stress analysis) increased in our angina physiology model but not with ischemia of the coronary occlusion type? (5) Does the end diastolic LV pressure-segment length relation (obtained from vena caval occlusions) show similar changes to the dynamic (multiple points from a single diastole) pressure-segment length relation with ischemia? (6) Does RV distension contribute to the upward shift in LV diastolic pressure-segment length relations in our angina physiology model? (7) Do decreases in myocardial high energy phosphates (serial biopsies) develop in a time course paralleling the diastolic abnormalities? (8) Are the myocardial relaxation abnormalities in this angina physiology model associated with a net increase in tissue Ca++ content (as in prolonged global ischemia)? (9) Do differences in lactate, pH, and p02 in coronary venous blood correlate well with the presence (angina model) or absence (coronary occlusion model) of major diastolic abnormalities?